HSD17B11 Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human near-haploid HAP1 cell line, offering a targeted loss-of-function model for the HSD17B11 gene. Created through CRISPR/Cas9-mediated gene disruption, this product contains a heterogeneous pool of edited cells, avoiding the biases associated with clonal isolation and enabling robust bulk functional analyses. The polyclonal format is particularly suited for studies where population-level responses are desired, such as metabolic profiling and hormone signaling assays, without the need for single-cell cloning.
HAP1 cells originate from the KBM-7 chronic myeloid leukemia cell line and possess a near-haploid karyotype, making them a widely adopted hematopoietic platform for genetic screens and functional genomics. Their haploid genome simplifies the interpretation of knockout phenotypes, as single-gene disruptions can yield clear and reproducible effects. These cells retain key characteristics of the leukemic lineage and are routinely employed in signal transduction research, cancer biology, and drug target validation, providing a physiologically relevant context for studying genes involved in hormone and lipid metabolism.
HSD17B11 encodes a 17??-hydroxysteroid dehydrogenase that primarily catalyzes the oxidation of active androgens and estrogens to their less potent keto forms, including the conversion of testosterone to androstenedione and estradiol to estrone. The enzyme is regulated upstream by androgen receptor signaling, PPAR??, and SREBP1c, and it requires NAD+ or NADP+ as cofactors. Beyond steroid metabolism, HSD17B11 participates in retinol oxidation, producing retinaldehyde from retinol, and interacts with PLIN2, a lipid droplet scaffold protein, thereby linking hormone regulation to lipid droplet homeostasis. This dual functionality positions HSD17B11 at a critical node between endocrine signaling and cellular lipid management.
In the HAP1 polyclonal knockout model, disruption of HSD17B11 impairs the inactivation of sex steroids, potentially leading to heightened androgen and estrogen activity that could influence leukemic cell growth and differentiation. The loss of retinol-to-retinaldehyde conversion may also affect retinoid signaling pathways. Furthermore, compromised interaction with PLIN2 likely disturbs lipid droplet dynamics, which is particularly relevant given the emerging role of lipid metabolism in cancer cell survival. This knockout thus provides a versatile tool to investigate how hormonal and metabolic cues intersect in a hematopoietic cancer background.
Researchers can apply this polyclonal knockout population in a wide array of experimental contexts. Molecular validation via Western blotting and RT-qPCR confirms HSD17B11 depletion, while LC-MS-based steroid profiling quantifies changes in key hormones like testosterone and estradiol. Lipid droplet visualization with BODIPY staining and cell proliferation assays under varied hormonal conditions enable functional characterization of metabolic and proliferative phenotypes. The model supports investigations into steroid hormone biology, endocrine cancers (notably prostate cancer), obesity, metabolic syndrome, and lipid droplet dynamics. For further technical details, please contact Ascent Research.
